Why the study?
Whether lethal cardiomyopathy seen in global Sorbs2 knockout mice stems from intrinsic cardiomyocyte loss of Sorbs2 remained unknown, and its clinical relevance in human cardiomyopathy was underexplored.
Does cardiomyocyte-specific deletion of Sorbs2 lead to dilated cardiomyopathy and heart failure in mice?
Population
Mice with cardiomyocyte-specific loss of Sorbs2 (Sorbs2-cKO)
Comparison
Cardiomyocyte-specific deletion of Sorbs2 vs control
Design
Preclinical animal and translational study
Follow-up
Approximately one year of age
Authors
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Cardiomyocyte Sorbs2 loss may drive cardiomyopathy in mice; leaves open human relevance and mechanisms.
Does cardiomyocyte-specific deletion of Sorbs2 lead to dilated cardiomyopathy and heart failure in mice?
Sorbs2 is essential for maintaining cytoskeletal structural integrity in cardiomyocytes, and its loss leads to progressive dilated cardiomyopathy and heart failure in mice.
McLendon et al. (2022) studied this question.
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